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更新于：2025-04-03
Icaritin
阿可拉定
更新于：2025-04-03
概要
基本信息
原研机构 |
非在研机构- |
最高研发阶段批准上市 |
首次获批日期 中国 (2022-01-10), |
最高研发阶段(中国)批准上市 |
特殊审评优先审评 (中国)、附条件批准 (中国) |
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关联
26
项与 阿可拉定 相关的临床试验NCT06896396
Icaritin Soft Capsules and TACE Combined with Immunotherapy and Targeted Therapy Versus TACE Combined with Immunotherapy and Targeted Therapy for Unresectable Hepatocellular Carcinoma：a Prospective, Double-arm, Exploratory Study
NCT06893887
Exploratory Cohort Study and Mechanistic Research on Individualized Comprehensive Treatment After Standard Treatment for Advanced Hepatocellular Carcinoma
NCT06825546
A Multicenter Study Assessing the Efficacy and Safety of Icaritin in Combination With AG Chemotherapy Versus AG Chemotherapy Alone in Patients With Previously Untreated Advanced Pancreatic Ductal Adenocarcinoma
100 项与 阿可拉定 相关的临床结果
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100 项与 阿可拉定 相关的转化医学
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100 项与 阿可拉定 相关的专利（医药）
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344
项与 阿可拉定 相关的文献（医药）2025-08-01JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS
Comprehensive characterization of the chemical composition of Ela tablet and its metabolites, with molecular docking screening of potential bioactive components for erectile dysfunction treatment
Article
作者: Liu, Yongqiang ; Xi, Ruqi ; Aisa, Haji Akber ; Abdulla, Rahima
Erectile dysfunction (ED) is a disorder involving both physiological and psychological implications, and phosphodiesterase 5 (PDE5) inhibitors serve as the primary treatment. The Ela tablet, a traditional herbal formulation, has demonstrated promising PDE5 inhibitory effects, yet its bioactive constituents and metabolic fate remain unclear. A four-step strategy combining offline two-dimensional supercritical fluid chromatography (SFC) and ultra-high-performance liquid chromatography coupled with high-resolution mass spectrometry (UHPLC-HRMS) was established to characterize the chemical composition of the Ela tablet. This was followed by in vivo metabolic profiling in rats to determine prototype compounds and metabolites. Molecular docking analysis was then conducted to evaluate the interaction of blood-absorbable prototype compounds with PDE5. A total of 362 compounds were identified, including flavonoids, alkaloids, terpenoids, organic acids and other classes of compounds. In vivo metabolic profiling revealed 70 compounds of prototype and metabolites, with hydrolysis and glucuronidation as the predominant metabolic pathway. Icaritin glycoside analogs underwent extensive metabolism producing Icaritin glucuronide conjugates as the major circulating forms, while N-alkylamides primarily remained in their prototype state. Molecular docking analysis revealed N-isobutyl-(2E,4E)-tetradecadienamide, Anacyclin, Dodeca-2E,4E-dienoic acid isobutylamide, Pellitorine, N-isobutyl-2-6-8-decatrienamide, Icaritin, and Desmethylicaritin as potential PDE5 inhibitors. These findings provide insights into the metabolic transformation and pharmacological mechanisms of the Ela tablet, supporting its potential clinical application in ED treatment. Future research should focus on pharmacokinetics, mechanistic validation, and clinical evaluation to further establish its therapeutic efficacy.
2025-06-01PHYTOMEDICINE
The pathogenesis of hepatocellular carcinoma: ERK/ULK1/NCOA4-mediated inhibition of iron autophagy, and Epimedium extract targeted modulation of this pathway to treat hepatocellular carcinoma
Article
作者: Yang, Xinxin ; Bao, Yongrui ; Li, Tianjiao ; Han, Liying ; Meng, Xiansheng ; Tian, Xiangmu ; Wang, Shuai
BACKGROUND:
The pathogenesis of hepatocellular carcinoma (HCC) is characterized by its complexity and diversity, involving processes such as glycolysis, autophagy, and cellular immunity. Notably, the role of ERK/ULK1/NCOA4-mediated inhibition of iron autophagy in HCC pathogenesis has not been previously reported. This study provides a novel elucidation of HCC pathogenesis and identifies the clinical adjuvant therapy drug, Epimedium, as a potential treatment based on this mechanism. The research clarifies the regulatory effects of Epimedium on the ERK/ULK1/NCOA4-mediated inhibition of iron autophagy pathway in the treatment of HCC, thereby offering a scientific foundation for clinical treatment strategies and the development of innovative drugs.
PURPOSE:
The objective of this study is to uncover a new aspect of HCC pathogenesis, ERK/ULK1/NCOA4-mediated inhibition of iron autophagy, and to screen for clinical targeted adjuvant therapy drugs based on this mechanism.
METHODS:
A HCC rat model was induced with N-Nitrosodiethylamine (DEN). The physiological status of the HCC rats was assessed through indicators such as body weight and organ index. Liver damage in HCC rats was evaluated using hematoxylin and eosin (HE) staining and biochemical markers. Additionally, untargeted metabolomics was employed to explore the pathogenesis of HCC. UPLC-Q-TOF-MS combined with network pharmacology was employed to elucidate novel mechanisms, predict pathway targets, filtrate active ingredients and analyze the biological processes and signaling pathways modulated by EPME. DEN liver cancer rats were treated with different concentrations of EPME and protein expression levels were assessed by Western blot analysis. Molecular docking techniques were utilized to assess the binding affinity between the core components of EPME and target proteins. A HepG2 liver cancer in vitro model, in combination with inhibitor (SBI-0206965), was employed to verify the modulatory effects of EPME and its active ingredients on the ERK/ULK1/NCOA4 signaling pathway. Microscale thermophoretic (MST) was employed to verify the binding ability of the EPME core components to the ULK1 protein.
RESULTS:
Metabolomics combined with network pharmacology revealed a novel pathogenesis of HCC, which is ERK/ULK1/NCOA4-mediated iron autophagy inhibition. EPME can activate iron autophagy mediated by ERK/ULK1/NCOA4 through active ingredients such as icaritin, astragalin, and emodin, thereby enhancing the survival conditions of HCC-afflicted rats and mitigating liver damage and carcinogenesis, ultimately achieving therapeutic outcomes in HCC treatment.
CONCLUSION:
The ERK/ULK1/NCOA4-mediated iron autophagy inhibition represents a novel therapeutic mechanism for HCC. The clinical adjuvant drug EPME may exert therapeutic effects on HCC by activating ERK/ULK1/NCOA4-mediated iron autophagy.
2025-04-01APOPTOSIS
Integrating single-cell sequencing and machine learning to uncover the role of mitophagy in subtyping and prognosis of esophageal cancer
Article
作者: Liang, Yiwei ; Gao, Yaxian ; Hu, Minxuan ; Tian, Feng ; Wang, Zijie ; He, Xinyang ; Wang, Saiwei
Globally, esophageal cancer stands as a prominent contributor to cancer-related fatalities, distinguished by its poor prognosis. Mitophagy has a significant impact on the process of cancer progression. This study investigated the prognostic significance of mitophagy-related genes (MRGs) in esophageal carcinoma (ESCA) to elucidate molecular subtypes. By analyzing RNA-seq data from The Cancer Genome Atlas (TCGA), 6451 differentially expressed genes (DEGs) were identified. Cox regression analysis narrowed this list to 14 MRGs with potential prognostic implications. ESCA patients were classified into two distinct subtypes (C1 and C2) based on these genes. Furthermore, leveraging the differentially expressed genes between Cluster 1 and Cluster 2, ESCA patients were classified into two novel subtypes (CA and CB). Importantly, patients in C2 and CA subtypes exhibited inferior prognosis compared to those in C1 and CB (p < 0.05). Functional enrichments and immune microenvironments varied significantly among these subtypes, with C1 and CB demonstrating higher immune checkpoint expression levels. Employing machine learning algorithms like LASSO regression, Random Forest and XGBoost, alongside multivariate COX regression analysis, two core genes: HSPD1 and MAP1LC3B were identified. A prognostic model based on these genes was developed and validated in two external cohorts. Additionally, single-cell sequencing analysis provided novel insights into esophageal cancer microenvironment heterogeneity. Through Coremine database screening, Icaritin emerged as a potential therapeutic candidate to potentially improve esophageal cancer prognosis. Molecular docking results indicated favorable binding efficacies of Icaritin with HSPD1 and MAP1LC3B, contributing to the understanding of the underlying molecular mechanisms of esophageal cancer and offering therapeutic avenues.
100 项与 阿可拉定 相关的药物交易
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外链
| KEGG | Wiki | ATC | Drug Bank |
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| - | - | - |
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 肝细胞癌 | 中国 | 2022-01-10 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 不可切除的肝细胞癌 | 临床3期 | 中国 | 2022-12-12 | |
| 肝癌 | 临床3期 | 中国 | 2022-01-30 | |
| 晚期肝细胞癌 | 临床3期 | 中国 | 2017-09-08 | |
| 乙型肝炎病毒相关肝细胞癌 | 临床3期 | 中国 | 2017-09-08 | |
| 晚期癌症 | 临床1期 | 中国 | 2011-11-28 | |
| 晚期恶性实体瘤 | 临床1期 | 中国 | 2011-11-01 | |
| 晚期乳腺癌 | 临床1期 | 中国 | 2010-11-01 | |
| 转移性乳腺癌 | 临床1期 | 中国 | 2010-11-01 | |
| 错配修复缺陷或微卫星高度不稳定性结直肠癌 | 临床申请批准 | 中国 | 2025-03-04 |
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临床结果
临床结果
适应症
分期
评价
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临床3期 | 283 | 網窪積鑰製蓋獵艱餘蓋(齋鏇糧鏇齋選顧艱觸糧) = 艱繭膚糧積顧築積觸鏇 觸襯壓艱獵餘繭遞憲觸 (齋廠壓獵壓觸衊顧艱夢 ) 更多 | 积极 | 2021-05-20 | |||
huachashu | 網窪積鑰製蓋獵艱餘蓋(齋鏇糧鏇齋選顧艱觸糧) = 願遞顧遞鬱顧鹹壓鑰簾 觸襯壓艱獵餘繭遞憲觸 (齋廠壓獵壓觸衊顧艱夢 ) 更多 | ||||||
临床1期 | 20 | 觸壓鏇鏇醖鏇襯顧網顧(鬱壓願蓋艱鑰鬱鏇築鏇) = 蓋築構構繭鏇鹹積襯鹽 艱齋憲鹽鑰願膚醖範淵 (齋壓顧構積製憲窪餘範 ) 更多 | 积极 | 2019-03-28 | |||
N/A | - | - | 襯顧衊觸範顧壓鬱鹽獵(築憲繭艱艱鏇窪範窪獵) = 醖襯鑰膚衊憲遞淵淵願 壓齋壓餘襯觸積蓋積齋 (鹹遞繭選餘鬱範繭製蓋 ) 更多 | 积极 | 2015-04-17 |
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